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Myocardial tumour necrosis factor-alpha (TNF-alpha) production plays an important role in cardiac dysfunction during sepsis. The aim of this study was to investigate the role of c-Jun NH2-terminal kinases (JNK) signalling in cardiomyocyte TNF-alpha expression during lipopolysaccharide (LPS) stimulation and myocardial function in endotoxaemic mice.

JNK1/c-fos inhibits cardiomyocyte TNF- expression via a negative crosstalk with ERK and p38 MAPK in endotoxaemia